OBJECTIVE: The aim was to test the hypothesis that adrenaline affects the force-interval processes. METHODS: The force-interval processes were studied in eight guinea pig papillary muscles (isometric force) and five anaesthetised dogs with atrioventricular block (maximum rate of rise of left ventricular pressure, LVdP/dtmax). The contractility indices were measured during pacing sequences in which a steady state was interrupted after a variable interval by a premature beat followed by an immediate return to the steady state. RESULTS: The relationship between contractility of the premature beat and the preceding interstimulus interval displays an approximately monoexponential initial rising phase, ie, mechanical restitution. With increasing adrenaline dosage in the isolated preparation there was always a significant increase in the force, and in its rate of rise with interval in some cases. Adrenaline had a variable accelerating effect on the time course of this mechanical restitution in isolated papillary muscles, but no effect in the dog preparation. In the isolated preparation adrenaline also slowed the decay in potentiation of the two beats immediately following the premature contraction. A slope of the relationship between the contractility of the second potentiated beat and that of the first was thus increased. This difference was not apparent in the intact preparation. CONCLUSIONS: The speeding up of mechanical restitution by adrenaline may be interpreted as reflecting the time course of reavailability of contractile activator. The slope of the relationship of contractility to that of the previous beat during the decay of postextrasystolic potentiation may be interpreted as the recirculation fraction of contractile activator; this is increased by adrenaline. However, in addition, adrenaline exerts an inotropic effect by another mechanism.
OBJECTIVE: The aim was to test the hypothesis that adrenaline affects the force-interval processes. METHODS: The force-interval processes were studied in eight guinea pig papillary muscles (isometric force) and five anaesthetised dogs with atrioventricular block (maximum rate of rise of left ventricular pressure, LVdP/dtmax). The contractility indices were measured during pacing sequences in which a steady state was interrupted after a variable interval by a premature beat followed by an immediate return to the steady state. RESULTS: The relationship between contractility of the premature beat and the preceding interstimulus interval displays an approximately monoexponential initial rising phase, ie, mechanical restitution. With increasing adrenaline dosage in the isolated preparation there was always a significant increase in the force, and in its rate of rise with interval in some cases. Adrenaline had a variable accelerating effect on the time course of this mechanical restitution in isolated papillary muscles, but no effect in the dog preparation. In the isolated preparation adrenaline also slowed the decay in potentiation of the two beats immediately following the premature contraction. A slope of the relationship between the contractility of the second potentiated beat and that of the first was thus increased. This difference was not apparent in the intact preparation. CONCLUSIONS: The speeding up of mechanical restitution by adrenaline may be interpreted as reflecting the time course of reavailability of contractile activator. The slope of the relationship of contractility to that of the previous beat during the decay of postextrasystolic potentiation may be interpreted as the recirculation fraction of contractile activator; this is increased by adrenaline. However, in addition, adrenaline exerts an inotropic effect by another mechanism.
Authors: S Hosogi; J Araki; Y Syuu; S Suzuki; S Mohri; T Mikane; H Matsubara; T Ohe; M Hirakawa; H Suga Journal: Heart Vessels Date: 1997 Impact factor: 2.037